Abstract
Nuclear factor erythroid-2–related factor-2 (NFE2L2/Nrf2) is a transcription factor that regulates the expression of antioxidant genes. Both Kelch-like ECH-associated protein 1 (Keap1) mutations and Nrf2 mutations contribute to the activation of Nrf2 in non-small cell lung cancer (NSCLC). Nrf2 activity is associated with poor prognosis in NSCLC. Metabolic reprogramming represents a cancer hallmark. Increasing studies reveal that Nrf2 activation promotes metabolic reprogramming in cancer. In this review, we discuss the underlying mechanisms of Nrf2-mediated metabolic reprogramming and elucidate its role in NSCLC. Inhibition of Nrf2 can alter metabolic processes, thus suppress tumor growth, prevent metastasis, and increase sensitivity to chemotherapy in NSCLC. In conclusion, Nrf2 may serve as a therapeutic target for the treatment of NSCLC.
Highlights
Lung cancer is the leading cause of cancer-related death worldwide [1]
Most NADPH-related genes are regulated by Nrf2, including four NADPH generating enzymes glucose-6-phosphate dehydrogenase (G6PD), isocitrate dehydrogenase (IDH1), malic enzyme 1 (ME1), and phosphogluconate dehydrogenase (PGD)
Metabolic reprogramming of tumor cells has undergone drastic discussions during the past decade
Summary
Nuclear factor erythroid-2–related factor-2 (NFE2L2/Nrf2) is a transcription factor that regulates the expression of antioxidant genes. Both Kelch-like ECH-associated protein 1 (Keap1) mutations and Nrf mutations contribute to the activation of Nrf in non-small cell lung cancer (NSCLC). Nrf activity is associated with poor prognosis in NSCLC. Increasing studies reveal that Nrf activation promotes metabolic reprogramming in cancer. We discuss the underlying mechanisms of Nrf2-mediated metabolic reprogramming and elucidate its role in NSCLC. Inhibition of Nrf can alter metabolic processes, suppress tumor growth, prevent metastasis, and increase sensitivity to chemotherapy in NSCLC. Nrf may serve as a therapeutic target for the treatment of NSCLC
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